Schizophrenia - Flashcards

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1
Q

What is schizophrenia?

A

A severe mental illness where contact with reality and insight are impaired, an example of psychosis.

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2
Q

What percentage of general population suffer?

A

1%

Affects more men than women.

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3
Q

What are the 2 types of symptoms?

A

Positive - appear to reflect an excess or distortion of normal functions
Negative - appears to reflect loss of normal functions

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4
Q

What are the positive symptoms?

A

Hallucinations - auditory, aufactory (taste/smell), tactile (touch), visual.
Disordered thinking
Delusion - paranoid delusions, delusions of grandeur.

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5
Q

What are the negative symptoms?

A

Alogia (poverty of speech)
Avolition (reduction of goal directed behaviour)
Affective flattening (reduction in intensity and range of emotion)
Catatonic (immobile, withdrawn)
- Harder to treat
- Symptoms often co -morbid with depression.

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6
Q

Evaluation of diagnosis of schizophrenia?

A
  • Poor inter-rater reliability - Cheniaux 2009 had 2 psychiatrists diagnose 100 patients using DSM and ICD criteria - diagnosed differently for the same patient.
  • Poor criterion validity - Cheniaux found ICD is used more than DSM (under or over diagnosed).
  • Symptoms co - morbid - Buckley 2009 found those which schizophrenia were also, 50% diagnosed with depression, 47% substance abuse. We may not be correctly diagnosing.
  • Symptom overlap
  • Gender bias - Cotton 2009 says that women function better (why less diagnosed)
  • Culture bias
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7
Q

What is the genetic biological explanation for schizophrenia?

A

Genetic - Schiz runs in families MZ twin concordance rate 47% - DZ 17%. (Gottesman 1991).
Adoption studies - 30% concordance rate in relatives vs 15% adopted families (Tienari 1994).

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8
Q

What is the dopamine biological explanation for schizophrenia?

A

Brains chemical messengers work differently in schizophrenic.
Hyperdopaminergia in subcortex (high levels of dopamine) - Amphetamines increase dopamine levels and it causes hallucinations.
Hypodopaminergia in cortex (low levels) - abnormal dopamine systems in pre - frontal cortex. - Antipsychotic drugs reduce dopamine but too many causes ticks/tremas associated with Parkinson’s (causes by low levels of dopamine).
HIGH AND LOW LEVELS OF DOPAMINE ARE RESPONSIBLE FOR SCHIZOPHRENIA.

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9
Q

What is the neural correlate biological explanation for schizophrenia?

A

Patterns/structures of the brain which that correlate with schizophrenia suffers.
Negative symptoms - Juckel 2006 found low activity levels in the ventral striatum of schizophrenics; responsible for anticipation which would explain avolotition (loss of motivation) in suffers. Also found negative correlate of activity levels and severity of symptoms.
Positive symptoms - Allen 2007 found that reduced activity levels in the superior temporal gyrus and anterior cingulate gyrus related to auditory hallucinations.

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10
Q

Evaluation of biological explanations?

A

+ Evidence supports genetic factors - Gottesman twin study, Tienari adoption study. Ripke 2014 found particular genetic variations increase risk of schiz.

  • Mixed evidence for dopamine hypothesis + amphetamines and antipsychotics. - Ripke study suggests neurotransmitters like glutamate are also involved.
  • Correlation - causation - does unusual brain activity cause or a result of.
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11
Q

What is the biological therapy for schizophrenia?

A

Drug treatments. (works on dopamine)
Typical antipsychotics - Chlorpromazine - acts as an antagonist to dopamine (reduces). Blocks all dopamine receptors in synapse. Reduces positive symptoms and works as sedative. BAD SIDE EFFECTS.

Atypical antipsychotics - Clozapine - acts same as typical but also acts of serotonin and glutamate receptors to improve mood and cognitive functioning (blocks some receptors some of the time). Negative and positive symptoms. Works better on treatment - resistant patients (30 -50%). LESS BAD SIDE EFFECTS.

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12
Q

Evaluation of biological treatments?

A

+ Evidence of effectiveness - Thornley 2003 placebo study - found those with chlorprozamine had reduced symptoms and lower relapse rate.

  • Side effects - Tardive Dyskinesia (involuntary face movements) which is irreversible. Atypical less side effects but still careful of agranulocytosis.
  • Relies on dopamine hypothesis - may not be true, modern understanding almost opposite.
  • Problems with evidence - Healy 2012 exaggerated evidence as ignores long term effects (withdrawal)
  • Human rights abuse - not for patients benefit (calm them, easier to deal with)
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13
Q

What are the family psychological explanations for schizophrenia? 3

A

Schizophrenogenic mother - Frieda Fromm-Reichmann 1948. Suggests that this sort of mother is a contributing factor to schizophrenia. Characteristics include:
- Cold - Rejecting - Overprotective
- Rejecting - Uncaring.
Says this creates family tensions which later lead to distress and develop paranoid delusions.

Double Blind theory - Gregory Bateson 1972
Emphasised role of communication style within family.
Suggests child gets mixed messages about what is wrong and are punished with ‘withdrawal of love’. = confusing understanding of world which develops into disorganised thinking and paranoid delusions.

Expressed emotion
Level of emotion expressed (negative) towards patient by others.
- Verbal criticism - Hostility
- Emotional over-involvement in life of patient.
This high levels of EE is a source of stress - primary explanation for relapse in patients.

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14
Q

What is the cognitive psychological explanation for schizophrenia?

A

Frith 1992 - identified 2 kinds of irrational thought processes:
Meta - representation = inability to distinguish that our actions/thoughts are our own rather than someone else’s (explains hallucinations).
Central control = inability to control our responses e.g. cannot suppress automatic thoughts which triggers speech. Each word triggers further association (explains disorganised thinking).

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15
Q

Evaluation of psychological explanations for schizophrenia?

A

+ Evidence supports family explanation - Read 2005 found that 69% of women who suffered child abuse later developed schizophrenia.
+ Evidence support for cognitive - Stirling 2006, cognitive tasks, patients took twice as long to finish tasks than control group.

  • Problems with support for families - no support for schizophrenogenic mother or double blind.
  • Validity problems (families lie), ethics (blames parents)
  • Incomplete explanation (does not explain origins)
  • Ignores biological factors.
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16
Q

What is the psychological cognitive behavioural therapy (CBT)?

A

Involves helping patient identify irrational thoughts and change them. May be through:
- discussion of how likely beliefs are
- consideration of less threatening possibilities.
Does not cure schizophrenia but makes patients able to cope with it.

17
Q

What is the psychological family therapy?

A

Takes place in families rather than individual patients.
Aims to improve quality of communication and interaction between family members and reduce stress to prevent relapse (expressed emotion).
– Pharoah (2010) - reduce levels of stress and expressed emotion will increase chances of patients complying with medication.

18
Q

What is the psychological token economy therapy?

A

Token economy is reward system used to manage the behaviour of patients - especially those who have been institutionalised for long periods of time - to help re-introduce them back into everyday life.
- tokens are given to patients immediately when they have carried out a desirable behaviour for reinforcement. (immediate to prevent ‘delay discounting’ which would reduce effect).
– tokens can then be swapped for rewards.
This is based on operant conditioning.

19
Q

Evaluation of psychological therapies?

A

+ evidence for effectiveness -
Jauhar (2014) CBT has small effects on both positive and negative symptoms.
Pharoah - family therapy reduces relapse.
McMonagle and Sultana (2009) - token economies helped show improvement in patients.

  • evidence for effectiveness weak - McMonagle and Sultana: only 1 in 3 studies showed improvement and none showed useful information.
    Pharoah - studies were inconsistent
  • quality of research for effectiveness weak - poorly controlled conditions, conclusions optimistic.
  • treatments do not cure.
  • ethical issues - token economy, harder for patients with severe symptoms to gain rewards and may not work in real world.
20
Q

What is the interactionist approach to explaining schizophrenia?

A

Diathesis - stress model.
Says both a vulnerability to schizophrenia and a stress trigger are necessary to develop condition.
Meehl (1962) - entirely genetic, result of ‘schizogene’ which can be trigger through stress.
Modern understanding is that there is not just one gene but many and range beyond genetic - Ingram and Luxton (2005), trauma can be diathesis rather than stressor.
– Cannabis is seen to increase risk by up to 7 times.

21
Q

What is the interactionist therapy to schizophrenia?

A

Combines antipsychotic medication and psychological therapies, in particular CBT.
In Britain, is becoming increasingly standard practice - is a bit slower is USA.

22
Q

Evaluation of interactionist approach?

A

+ evidence for role of vulnerability and triggers - Tienari (2004) - 19,000 adopted, Finnish children with mothers schizophrenic between 1960 - 1979. Found link between genetic vulnerability and family stress in development of schizophrenia.
+ support for effectiveness of combinations of treatments - Tarrier (2004) patients in combination groups showed less symptoms than those is control group (medication only).

  • reductionist - (especially Meehl’s model).
  • incomplete - we don’t know how mechanisms work and how they are produced.
  • treatment-causation fallacy - just because biological approach and psychological approach combined work together doesn’t mean either are correct.